Reasons for performing study:Volatile fatty acids, byproducts of carbohydrate fermentation by resident bacteria, have been implicated in causing nonglandular (NG) gastric ulcers. Lactic acid (LA), also produced by stomach bacteria, may cause gastric ulcers when exposed to the equine NG mucosa.Summary
Objectives:To investigate thein vitroeffects of LA on equine NG mucosa bioelectric properties, sodium transport and tissue resistance.Summary
Methods:Gastric tissues obtained from 13 mature horses were studied in Ussing chambers. Short-circuit current (Isc) and potential difference (PD) were measured, and electrical resistance (R) and conductance (G) calculated for tissues after addition of HCl and LA (5, 10, 20 and 40 mmol/l) in normal Ringer's solution (NRS).Summary
Results:Mucosa exposed to HCl or LA (5, 10 and 20 mmol/l) in NRS (pH 1.5 and to a lesser extent pH 4.0) had a significant decrease in Isc and PD. Mucosa exposed to a high concentration of LA (40 mmol/l) in NRS (LRS) at pH 1.5 showed an increased G, but this increase was not significant. Values returned to baseline after solutions were returned to pH 7.0. Histological changes were consistent with HCl-induced (pH <4.0) acid damage.Summary
Conclusions:HCl induced alteration in bioelectric properties of equine NG mucosa whereas addition of LRS did not, other than those changes seen with HCl alone.Summary
Potential relevance:Lactic acid, produced in the stomach of horses fed a high-grain diet, does not significantly alter sodium transport or permeability in equine NG mucosal tissue. Lactic acid may require a longer exposure time or may need the presence of other VFAs in HCl to cause gastric ulcers.